1. Lung ILC2s link innate and adaptive responses in allergic inflammation
Itziar Martinez-Gonzalez, Catherine A. Steer, Fumio Takei 
Trends in Immunology 
Volume 36, Issue 3, Pages (March 2015)
DOI: /j.it
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2. Figure 1
Stimulation of group 2 innate lymphoid cells (ILC2s) by epithelium-derived cytokines leading to innate type 2 immunity. Inhaled allergens induce the release of the alarmins IL-33 and uric acid as well as the secretion of IL-25 and TSLP by the lung epithelium. IL-33 release may be promoted by PAR activation or by uric acid. Epithelial cells also produce IL-25, TSLP, and IL-7. IL-33 stimulates basophils to produce IL-4. Lung ILC2s are stimulated by combinations of IL-33, TSLP, IL-7, and IL-4 and produce type 2 cytokines including IL-5, IL-13, IL-9, and amphiregulin. These cytokines act on different types of cells promoting type 2 lung inflammation characterized by eosinophilia, mucus production, smooth muscle contraction, and airway hyper-reactivity. Abbreviations: AREG, amphiregulin; IgE, immunoglobulin E; IL, interleukin; PAR, protease-activated receptor; TSLP, thymic stromal lymphopoietin.
Trends in Immunology  , DOI: ( /j.it )
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3. Figure 2
Lung group 2 innate lymphoid cells (ILC2s) promote Th2 cell differentiation. Upon allergen activation, lung ILC2s produce IL-13, which promotes activated CD40+ dendritic cell (DC) migration to the draining mediastinal lymph node (mLN). DCs present antigen to naive CD4+ T cells and drive their differentiation into Th2 cells. Th2 cells then migrate to the lung and produce type 2 cytokines such as IL-4, IL-5, and IL-13 and induce allergic lung inflammation. Abbreviations: aDC, activated dendritic cell; iDC, immature dendritic cell; IL, interleukin; MHCII, major histocompatibility complex class II; mLN, mediastinal lymph node; TCR, T cell receptor; Th2, T helper type 2.
Trends in Immunology  , DOI: ( /j.it )
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